​Kembara Xtra - Medicine - Bell Palsy

​Kembara Xtra - Medicine - Bell Palsy 
Introduction:
Acute peripheral facial nerve palsy, typically unilateral.
Although the etiology is primarily idiopathic, type 1 of the herpes simplex virus (HSV) has been implicated in numerous cases.
The facial nerve being affected by an ischemic process has also been proposed as a potential cause of Bell palsy.

Epidemiology and Statistics: 0.002% of the population yearly; no geographic or gender predominance; affects all ages, with a median age of onset of 40 years; maximum incidence in people over 70 years; equally common on the left and right sides of the face; no geographic or gender predominance.
Incidence
The majority of population studies have revealed a 15–30 per 100,000 annual incidence.

Pathophysiology and Etiology 
Inflammation of cranial nerve VII results in edema of the perineurium, compression of the nerve, and perhaps degeneration of the accompanying vasa nervorum.
Activation of latent herpes viruses (HSV type 1 and herpes zoster virus) in cranial nerve ganglia is the most likely infectious cause among the postulated infectious, immunological, and ischemic mechanisms.

Risk factors include: Immunocompromised state; Diabetes mellitus; Age >30 years; Obesity; Chronic hypertension; Maternal obesity; Pregnancy, with higher risk reported in individuals with chronic hypertension, severe preeclampsia, and maternal obesity

Bell Palsy Detection and Diagnosis 
Bell palsy is identified through a thorough history and physical examination. When other differentials are likely based on the history and exam, labs and diagnostic imaging may be taken into consideration.

Introducing History
Onset: usually quick (within 24 to 48 hours)
Key characteristics include unilateral lower motor neuron-type facial weakness without any additional systemic or neurologic symptoms. Patients who complain of being unable to close their eyelids or discover liquids dripping from the affected side of their mouth may seek medical assistance. The condition is gradual, with peak weakness happening up to 3 weeks following the first day of weakness. It could take several months for symptoms to get better.
● Although facial weakness may be a sign of a stroke, this is not frequently the case. Additionally, Bell palsy-mimicking stroke lesions (affecting the ipsilateral facial nerve nucleus or facial nerve tract in the pons) are extremely uncommon.
● Alongside symptoms:
- Postauricular or mastoid discomfort - Hyperacusis: heightened acuity (nerve to the stapedius muscle)
- Dysgeusia, which affects the taste buds on the ipsilateral anterior third of the tongue (chorda tympani branch of the facial nerve).
- Ipsilateral side of the face numbness - Reduced salivation or lacrimation (parasympathetic effects)
A more likely cause of the patient's facial nerve paralysis, such as herpes zoster, Lyme disease, or sarcoidosis, may be discovered by inquiring about the patient's travel history, whether they have lived in a region where Lyme disease is endemic, or whether they have any skin rashes.

clinical assessment 

Inability to raise the ipsilateral brow, close the ipsilateral eye, or smile, grin, or purse the lips due to flaccid paralysis of the muscles on the affected side, particularly those in the forehead.
The Bell phenomenon is when the eye turns upward while trying to close its lid.
Determine whether the weakness is due to a central (upper motor neuron) or peripheral (lower motor neuron) lesion. Unlike low motor neuron lesions, higher motor neuron lesions typically spare the forehead muscles.
– Patients may report feeling numb, but sensory testing reveals no loss.
– Other cranial nerves, including the trigeminal, glossopharyngeal, and hypoglossal, may have slight abnormalities; however, if these symptoms are obvious, Bell palsy is unlikely to be the cause.
Carefully inspect the head, ears, eyes, nose, and throat (HEENT) to rule out any lesions that are space-occupying.
– Conduct a pneumatic otoscopy examination.
Check the skin for vesicular rash (herpes zoster virus) and erythema migrans (Lyme disease).

Multiple Diagnoses 

 Bell palsy may not be the cause of up to 50% of cases with peripheral facial nerve palsy.
● If any of the "red flags" below apply, take into account additional differential diagnoses for peripheral facial nerve palsy:
- Weeks to months of gradual onset - Coexisting vertigo or hearing loss
- Cervical lymphadenopathy and/or constitutional symptoms
- Lyme disease symptoms - A failure to improve within 3 months or a worsening of weakness over a period of months.
● Etiologies of facial cranial nerve palsy include:
- Congenital reasons include genetic disorders, birth trauma, and facial muscular hypoplasia.
- Acquired causes include inflammatory (vasculitis, sarcoidosis, autoimmune), neoplastic (benign, malignant), cerebrovascular (stroke, aneurysm), and traumatic (Ramsay Hunt syndrome, Lyme disease, TB, HIV).
Clinical strategy based on the pattern of facial palsy
- Neoplasm of the nerve (schwannoma) or other structures (parotid, temporal bone, or cerebellopontine angle [CPA]) may cause recurrent, ipsilateral palsy.
- Neurologic conditions (Guillain-Barré syndrome) or neoplasms (lymphoma, disseminated carcinomatosis, malignant pachymeningitis) can cause bilateral palsy; uncommon conditions include cryptococcal meningitis linked with HIV, autoimmune conditions (MS, myasthenia gravis, Sjögren's syndrome), sarcoidosis, and granulomatosis with polyangiitis.
Segmental developmental palsy (linked to synkinesis, recovers on its own) is a palsy that occurs at birth.
- Facial palsy syndromes: Heerfordt-Waldenström (parotid enlargement, anterior uveitis, facial palsy, and fever); Melkersson-Rosenthal (orofacial edema, recurrent facial palsy, and fissured tongue); Ramsay-Hunt (rash in the ear [zoster oticus] and/or mouth caused by VZV);

Diagnostic Test Interpretation 
 A clinical diagnosis is bell palsy. Diagnostic imaging or standard lab tests are not required in those with newly developed Bell palsy. 
However, in the following cases, additional testing may be thought about: Facial palsy with an unusual presentation
 Slowly progressing illness lasting more than three weeks Lack of improvement after four months
Initial 

Lab and imaging tests

Blood sugar level, CBC, CRP/ESR, and other tests to rule out inflammatory processes
If necessary, take into account a rapid plasma reagin (RPR), Lyme serology, and/or an HIV test.
Think about your hepatitis A, B, C, CMV, VZV, rubella, and titers for these viruses.
Salivary polymerase chain reaction (PCR) for the herpes zoster virus or HSV-1 (primarily for research purposes)


Tests in the Future & Special Considerations
Invasive diagnostic treatments are not advised because biopsy could further harm the nerve. Trauma: facial radiography to evaluate for fractures; Contrast-enhanced CT to evaluate for stroke or temporal bone fracture; Gadolinium-enhanced MRI to evaluate for brain or parotid neoplasms.

Other/Diagnostic Procedures
Patients with total paralysis may be given electrodiagnostic tests for prognostic purposes, although this does not alter the therapy.
If there is no improvement and imaging is negative after 7 months, a parotid gland biopsy may be undertaken.
Management 
Generally Speaking 
To lubricate the cornea, artificial tears should be used often.
To prevent dryness and infection, the ipsilateral eye should be covered or taped shut at night.

Medication 

lacking treatment, Bell's palsy can be cured, especially in people lacking a full-blown palsy.
Corticosteroids reduce inflammation and minimize nerve damage, increasing the proportion of patients who recover completely and lowering the incidence of debilitating side effects (NNT = 10).
The use of antivirals as a monotherapy in new-onset Bell palsy is not advised because they have no advantage over placebo.
● Antivirals (in addition to steroids) may be given to individuals with newly developed Bell palsy in order to improve their chances of regaining facial function, according to a 2012 American Academy of Neurology (AAN) guideline (Level C evidence). Patients who are offered antivirals should be informed that their benefits have not been proven, and even if they do, they are most likely to be minimal.

Corticosteroids are advised in every incidence of Bell palsy.- Must begin within 72 hours of the appearance of symptoms– It is advised to take oral steroids for 10 days. Prednisolone 50 mg PO daily for 10 days is one option, as is Prednisone 60 mg daily for 5 days before weaning off by 10 mg/day for the next 5 days.
- Caution: Patients with diabetes and peptic ulcer disease should use this medication with caution.
- Contraindications include known hypersensitivity and underlying illnesses (TB, systemic mycosis).
Consider using valacyclovir 1,000 mg PO TID for 7 days if an antiviral is being utilized. Another choice is acyclovir, however it has a lower bioavailability.
- Caution: Patients with chronic kidney disease should use this medication with caution.
Use caution when using steroids when pregnant; speak with an obstetrician. The U.S. FDA classifies acyclovir and valacyclovir as Category B medications during pregnancy.

Motives for the Referral 

Consult a facial nerve specialist if you notice any worsening neurologic findings, any development of ocular problems, or any incomplete recovery three months from the start of your initial symptoms.

Further Therapies 
Electrostimulation and mirror biofeedback therapy provide scant evidence of benefit compared to drug treatment alone. There is insufficient evidence that physical therapy combined with medicinal treatment improves recovery.
Strong stimulation acupuncture has demonstrated some therapeutic promise, but no firm advice has been given.

Surgical procedures are only used in the most severe cases of Bell palsy and are still debatable.
To determine whether surgical surgery is helpful or harmful in the management of Bell palsy, there is not enough evidence.
Decompression surgery should not be performed more than 14 days after the onset of paralysis because severe degeneration of the facial nerve is likely irreversible after 2 to 3 weeks. In those cases where surgical intervention is performed, cranial nerve XII is surgically decompressed at the entrance to the meatal foramen where the labyrinthine segment and geniculate ganglion reside.

Patient Follow-Up Monitoring
Patients who do not fully regain facial nerve function should be referred to ENT and/or ophthalmology specialist(s) for further management. Start steroid treatment right away and follow up for 12 months.

The majority of patients recover fully spontaneously within 2 weeks, and >80% do so within 3 months.
85% of people who go untreated will start to feel better three weeks after their symptoms started.
A partial palsy, motor synkinesis, and autonomic synkinesis are left in 16% of patients, while recurrence may occur in 7% of cases on the afflicted or unaffected side, severe sequelae impact 5% of patients, and persistent facial weakness and dysfunction affect 1% of patients.
Clinical prognostic methods like the Sunnybrook and House-Brackmann (H-B) facial grading systems can tell which Bell palsy patients are most likely to stop improving after a year.
The following are some indicators of a poor prognosis:
Age >60 years, recurrence history, complete facial weakness, diabetes, high blood pressure, and House-Brackmann (H-B) grade II
The Sunnybrook score and corticosteroid treatment both significantly predict nonrecovery at one month.
Patients who don't get better or whose symptoms worsen should be sent to an ENT specialist; they could also need MRI to rule out neoplasms.

Complications include avascular necrosis of the hips, knees, and/or shoulders, steroid-induced hyperglycemia, corneal abrasion or ulceration, and psychiatric disorders.

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